T-cell receptor Vbêta gene segment expression in diisocyanate-induced occupational asthma.
Diisocyanates are the most common cause of occupational asthma induced by low-molecular-weight chemicals.
The disease appears to be immunologically, mediated but is independent of IgE antibody synthesis.
An underlying genetic susceptibility is suggested by the fact that the disease only develops in approximately 5% to 10% of exposed workers.
The study was designed to determine whether disease susceptibility is influenced by HLA and T-cell receptor Vbêta gene segment usage.
T-cell receptor Vbêta gene repertoires were quantitated by using primer pairs specific for Vbêta gene segments in conjunction with a common Cbêta region primer.
One group of workers with diisocyanate-induced occupational asthma produced diisocyanate-specific IgG and IgE antibodies, whereas the other group did not produce specific antibodies.
Occupational asthma was previously confirmed by either workplace challenge or laboratory speciflc diisocyanate bronchoprovocation.
Control groups consisted of diisocyanate-exposed workers who were free of symptoms, patients with nonoccupational asthma, and unexposed subjects who were free of symptoms.
Lymphocytes from workers with diisocyanate-induced occupational asthma had significantly decreased Vbêtal and Vbêta5 gene segment expression before in vitro exposure to diisocyanates compared with control groups. (...)
Mots-clés Pascal : Asthme, Pathogénie, Etiologie, Exposition professionnelle, Diisocyanate organique, Etats Unis, Amérique du Nord, Amérique, Récepteur cellule T, Région variable, Chaîne peptidique bêta, Système HLA, Système histocompatibilité majeur, Toxicité, Composé chimique, Immunité cellulaire, Homme, Maladie professionnelle, Médecine travail
Mots-clés Pascal anglais : Asthma, Pathogenesis, Etiology, Occupational exposure, Organic diisocyanate, United States, North America, America, T cell receptor, Variable region, Beta-Peptide chain, HLA-System, Major histocompatibility system, Toxicity, Chemical compound, Cellular immunity, Human, Occupational disease, Occupational medicine
Notice produite par :
Inist-CNRS - Institut de l'Information Scientifique et Technique
Cote : 97-0193903
Code Inist : 002B03L06. Création : 21/05/1997.